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Biomedical subjects

B K Mookerjee

Publications and source records attributed to B K Mookerjee.

At least 37 records · Page 2Linked to original sources
PubMed1986

Some effects of flavonoids on lymphocyte proliferative responses.

A number of representative flavonoids reversibly inhibit human lymphocyte proliferative responses in a concentration-dependent manner. The flavonoids quercetin and tangeretin are most effective when added during the early phase of exposure of lymphocytes to the mitogenic stimuli but become progressively less effective when added after increasing lengths of time following stimulation, suggesting an early flavonoid-sensitive step(s) in cell activation. In the proliferative response to phytomitogens, they do not act by inhibiting the early increase in calcium influx. They do not augment cellular cyclic-AMP concentration in basal or phytomitogen-stimulated lymphocytes nor reduce its increment in the presence of inhibitors of phosphodiesterase. At concentrations inhibitory to the proliferative response, quercetin (but not tangeretin) inhibits the calcium-activated, phospholipid-dependent protein kinase (C kinase). Certain flavonoids powerfully inhibit the uptake of thymidine into phytomitogen-stimulated lymphocytes but do not directly affect incorporation of already transported thymidine into newly synthesized DNA.

Calcium↗
PubMed1986

The effects of flavonoids on human lymphocyte proliferative responses.

Flavonoids reversibly inhibit lymphocyte proliferative responses to phytomitogens, soluble antigens and phorbol esters by blocking an early event or events that follow stimulation. Quercetin and tangeretin inhibit thymidine transport in stimulated lymphocytes. These flavonoids reversibly inhibit antigen processing by monocytes and inhibit the expression of class II histocompatibility (DR) antigens in PBM cells.

Antigen-Presenting Cells↗
PubMed1985

Human recombinant interleukin-2 is mitogenic to human lymphocytes.

Reported herein are the results of studies demonstrating that purified recombinant human interleukin-2 (hrlL-2) is a potent mitogen for lymphocytes of healthy human donors. The specificity of the hrlL-2-induced response was defined in experiments in which mitogenicity of this T cell growth-promoting lymphokine was completely abrogated by blocking the T cell membrane receptor for IL-2 with the anti-Tac monoclonal antibody. Depletion of adherent mononuclear leukocytes markedly reduced lymphocyte reactivity to hrlL-2, but the response could be fully recovered by the addition of interleukin-1 (IL-1). Increased proliferative responses were observed using a combination of hrlL-2 and a monoclonal antibody OKT3 that defines a T cell membrane antigen. These studies demonstrate that hrlL-2, as with antigens and phytomitogens, may serve as the first signal of T cell proliferation.

Antibodies, Monoclonal↗
PubMed1985

Peritoneal permeability in the rat: modulation by microfilament-active agents.

A model of peritoneal dialysis in the rat was used to determine the effects of cytochalasins on ultrastructure and peritoneal permeability to molecules of varying molecular weight. The permeability to urea, inulin, and plasma albumin were determined after intraperitoneal administration of cytochalasin B (2 to 10 X 10(-6) M) and cytochalasins D and E (2 X 10(-6) M). Cytochalasin B (20 X 10(-6) M) increased the permeability to inulin, urea, and albumin by 30, 60, and 150%, respectively. These effects were, to a large degree, reversible. Cytochalasins D and E produced greater increments in permeability for all molecules; this increase was only partially reversible. Ultrastructure analysis by scanning electron microscopy revealed extensive development of membrane protuberances (zeiotic knobs) on mesothelial cells exposed to cytochalasin B. A return to a normal apical cell surface was apparent although incomplete at 24 hr. Tight junctions were not grossly altered and major changes in intramembranous junctional strands were not observed. The major effect of cytochalasins on the cell surface may be responsible for the increased permeability to urea, predominately a transcellular probe. Inulin, which follows a paracellular route, was less affected. Altered protein permeability may be due to the action of cytochalasin on the exposed capillary endothelium in subdiaphragmatic areas where the mesothelium is discontinuous.

Animals↗
PubMed1984

Chemiluminescence and lymphocyte proliferation: parallelism in collaboration between subpopulations of thymus cells for both types of responses.

Rat thymocytes respond to exposure to phytomitogens by oxidant generation as detected by chemiluminescence in presence of luminol. Maximal chemiluminescent response to a wide variety of plant lectins was obtained only after the cells had been incubated for 18 hours at 37 degrees C but not at 4 degrees C. This temperature dependence and the necessity for intact protein-and RNA-synthetic machinery during the incubation period indicate the occurrence of differentiation of thymocytes as they develop the capacity for chemiluminescent response. Furthermore, adherent-phagocytic cells play an essential collaborative role during this differentiation. A remarkable parallelism was shown to exist in the capacity of a cell subset to respond to concanavalin A by DNA synthesis and the ability of the same subset to respond by chemiluminescence. The latest-sedimenting small lymphocytes after velocity sedimentation of thymus cells develop the capacity for DNA-synthetic as well as chemiluminescent responses to concanavalin A only if allowed to collaborate with a population of early-sedimenting adherent-phagocytic cells.

Animals↗
PubMed1984

Furosemide inhibits glucose transport in isolated rat adipocytes via direct inactivation of carrier proteins.

Furosemide inhibits 3-O-methyl-D-glucose equilibrium flux in isolated adipocytes. The inhibition is saturable with an increasing concentration of furosemide and shows a noncompetitive type of kinetics. Both basal and insulin-stimulated fluxes are equally affected by the inhibition. Hydrochlorothiazide and piretanide also inhibit the flux with a similar potency, whereas bumetanide, a more potent diuretic, is much less potent. To understand the molecular basis of this inhibition, effects of furosemide on the glucose-sensitive cytochaslasin B binding activities of adipocytes were studied. Furosemide inhibits the glucose-sensitive cytochalasin B binding of both microsomal and plasma membrane preparations. For both preparations, the inhibition is time dependent and only slowly reversible, is saturable with an increasing concentration of furosemide, shows a noncompetitive type of kinetics with apparent Ki (the inhibitor concentration that gives the half-maximum effect) of 3.5 and 0.7 mM after 2 and 18 h incubation, respectively, and is essentially identical between the basal and insulin-stimulated adipocytes. The inhibition develops with a first-order rate constant of approximately 0.12/h at 4 degrees C. These results indicate that furosemide inhibits glucose transport in adipocytes by directly inactivating transport carriers of both plasma membranes and microsomal reserve pool. This inactivation of glucose carrier may play a part in the diuretic-induced glucose intolerance frequently observed during diuretic therapy.

Adipose Tissue↗
PubMed1984

Effects of cytochalasins on lymphocytes: some distinctive features of cytochalasin-E.

Cytochalasin-E (CE) has specific properties that distinguishes it from other cytochalasin congeners. We have taken advantage of these in investigating the mechanisms operative in the effects of cytochalasins on lymphocyte proliferative responses to phytomitogens. Like the other cytochalasins, CE inhibits these responses only when present during the early phases of exposure of lymphocytes to mitogens, but not when added later on. The effects of CE are irreversible since prior incubation of lymphocyte in CE renders them incapable of response. Unlike the effects of cytochalasin A, the only other irreversibly active congener, lymphocytes preincubated in CE completely recover the ability to respond if they are cultured in cytochalasin-free medium for 48 hours. Unlike cytochalasins A and B, cytochalasin-E does not inhibit glucose transport into lymphocytes and all. We have shown that human lymphocytes bind cytochalasins at 3 distinct classes of sites named L, M, and H (J. Biol. Chem. 256:1290-1300, 1981). CE binds irreversibly to the L and H-sites on the short to medium term but does not bind to the glucose displaceable M-site at all. CE may have potential usefulness as affinity label towards isolation of specific binding sites since the chemical structure offers feasible approaches towards isotopic labelling.

Cytochalasins↗
PubMed1983

Ca2+ regulation of tight-junction permeability and structure in Necturus gallbladder.

To explore the role of Ca2+ in tight-junction permeability, the Necturus gallbladder was exposed to varying Ca2+ concentrations and to the Ca2+ ionophore A23187 added to the mucosal side (1.9 X 10(-6) to 6.8 X 10(-5) M). Electrophysiological parameters measured in an Ussing-type chamber were correlated with tight-junction morphology revealed by freeze-fracture electron microscopy. In Ca2+-free bathing media, transepithelial resistance decreases and tight-junctional ultrastructure is fragmented. In 1.8 mM Ca2+ media, A23187 induces an initial drop in transepithelial resistance, followed by an increase in transepithelial resistance to a value 20% above base line. At peak response to A23187, NaCl diffusion potentials decrease. Freeze-fracture replicas reveal that the number of junctional strands increase pari passu with junctional depth. Both physiological and morphological changes were partially reversible. The initial decrease in transepithelial resistance coincided with a persistent hyperpolarization of the mucosal cell membrane potential difference and a decrease in the mucosal-to-serosal cell membrane resistance ratio. Thus A23187 alters both the transcellular and paracellular pathway, resulting in opposing effects on transepithelial resistance.

Animals↗
PubMed1983

Effects of cytochalasins on lymphocytes: mechanism of inhibition of rosette formation.

The mechanisms operative in the inhibition by cytochalasins of human peripheral blood T lymphocytic rosette formation with sheep erythrocytes remain obscure in the light of the multiplicity of biologic effects of cytochalasins. Moreover, we have shown the existence of three distinct classes of cytochalasin-binding sites (H-, M-, and L-sites) in such lymphocytes (J. Biol. Chem. 256:1290-1300, 1981). We have, therefore, explored the mechanism of rosette inhibition and present evidence that shows: a) Inhibition of rosetting is not caused by inhibition of glucose transport in lymphocytes; b) cytochalasin binding to the H- and M-sites, both integral plasma membrane proteins, is not involved in the effect; c) nonspecific partitioning of cytochalasins in the plasma membrane lipids of lymphocytes appears unlikely to explain the effect; d) evidence presented in this paper strongly suggests that cytochalasin binding to the actin associated L-site mediates the inhibition of rosetting. We conclude that cytoskeletal microfilaments play a critical role in the normal functioning of cell surface receptors for binding to sheep erythrocytes.

Binding, Competitive↗
PubMed1982

Effects of diphtheria toxin and other exotoxins on oxidant generation by human and murine phagocytes.

Bacterial exotoxins such as diphtheria toxin (D.T.), staphylococcal alpha toxin and Leucocidin can powerfully activate granulocytes and macrophages as detected by production of chemiluminescence in presence of Luminol. Production of superoxide by granulocytes and of prostaglandin E2 in macrophages is also stimulated by D.T. In contrast with the known resistance of rodent parenchymal cells to the diphtheria toxin, human and rodent leucocytes have similar sensitivities to D.T.

Animals↗
PubMed1982

Hypertension in the elderly.

Successful control of blood pressure through drug therapy can reduce morbidity and mortality in the elderly population. However, age-related factors also make this group prone to adverse side effects. A cautious approach is therefore recommended in the effort to achieve ideal control of blood pressure.

Adrenergic beta-Antagonists↗
PubMed1981

The effects of cytochalasins on lymphocytes. Identification of distinct cytochalasin-binding sites in relation to mitogenic response and hexose transport.

Cytochalasin B inhibits phytomitogen-induced human lymphocyte proliferation with a Ki of approximately 6 X 10(-6) M. Cytochalasins A, C, D, E, and H are also inhibitory with varying degrees of potency, whereas cytochalasin G and chaetoglobosins A, B, C, E, F, and J are not at concentrations as high as 15 microM. Cytochalasin B also competitively inhibits carrier-mediated equilibrium exchange of hexose (Ki of approximately 7 X 10(-7) M), but cytochalasin E is ineffective. Cytochalasin B binds reversibly to the lymphocyte at three distinct sites: L, M, and H. The ligand binding at L site shows the apparent dissociation constant (Kd) of 1 to 3 X 10(-6) M and total binding sites (Bt) of 6 to 8 X 10(7)/cell, represents approximately 85% of the total saturable binding, displays a broad specificity interacting with cytochalasins C, D, and E, is not displaceable by D-glucose, is located mostly in a cytosol fraction, and exists in intimate relation to cytoskeletal actin. M site shows a Kd of 2 to 4 X 10(-7) M and Bt of 5 to 8 X 10(6)/cell, represents about 8% of the total saturable binding, shows stringent specificity not being displaced by cytochalasins C, D, and E, is competitively displaced by D-glucose and phloretin, and is quantitatively recoverable in the plasma membrane fraction. The binding to H site shows a Kd of 0.5 to 1.0 X 10(-7) M and Bt of 4 to 5 X 10(6)/cell, representing approximately 7% of the total saturable binding, shows a broad specificity, is insensitive to D-glucose, and is membrane bound. It is proposed that L site is actin and is involved in the inhibition of lymphocyte mitogenesis, whereas M site is associated with the hexose transport carrier. Structure-activity relationships of cytochalasin effects are also discussed.

Binding Sites↗
PubMed1981

Suppressed renin release during hyperoxia in the conscious dog.

Recent studies have documented a marked inhibition of renal prostaglandin E2 excretion during hyperbaric oxygenation (HBO) in the conscious dog. Numerous other studies have shown that pharmacological inhibition of prostaglandin synthesis is associated with diminished renin release. The current experiments were designed to test whether HBO is also accompanied by reduced renin secretory rate (RSR) in conscious dogs. Dogs were implanted with electromagnetic flow probes on the left renal artery as well as with chronic arterial and renal venous catheters. Renal blood flow, peripheral plasma renin activity, and renal venous renin activity were measured, which allowed calculation of RSR for the left kidney. The dogs were studied at normal atmospheric pressure while breathing room air, followed by exposure to 100% oxygen at 2 or 3 ATA. The dogs were then returned to room air. The RSR decreased from 153.6 +/- 51.6 (ng . h-1) . min-1 to 72 +/- 21 (ng . h-1) . min-1 during HBO. Upon return to normoxia, RSR rose to 345 +/- 140.4 (ng . h-1) . min-1. This renin response to HBO seems best related to the previously documented inhibition of renal prostaglandin synthesis. These experiments provide nonpharmacological evidence that there may be a functional relationship between the renin-angiotensin system and renal prostaglandin release in awake animals.

Animals↗
PubMed1980

Chemiluminescence and immune cell activation: general features of the thymocyte chemiluminescent responses to plant lectins.

Rat thymocytes respond to exposure to plant lectins by a burst of oxidant generation as detected by chemiluminescence (CL) (CL) in presence of luminol. All lectins tested were capable of evoking CL as long as sufficiently high concentration was used. There was no correlation between the capacity of a given lectin to evoke CL on one hand and its ability to cause mitogenic transformation or thymocyte agglutination on the other. During the first few minutes following exposure to Con A, cells in the thymocyte pool become committed to CL but once commitment is induced, removal of cell bound ligand by addition of excess methyl-alpha-D-mannoside does not significantly alter the response. Succinylated Con A is as effective as native Con A at lower concentrations but is much more effective at higher concentrations in evoking CL. Thymocyte CL can occur in absence of extracellular calcium but this calcium-independent CL is reduced by the addition of magnesium. In presence of calcium, CL response is greatly augmented and the calcium dependent response is not inhibited in presence of magnesium. The response is relatively radiosensitive. Thymocyte CL response is inhibitable by catalase and scavengers of oxidative radicals but is relatively resistant to the effects of superoxide dismutase, requiring high concentrations of significant effect.

Animals↗
PubMed1980

Antidiuresis and inhibition of PGE2 excretion by hyperoxia in the conscious dog.

Experiments were performed to determine the influence of varying inspired oxygen tension on renal prostaglandin E2 (PGE2) excretion, renal hemodynamics, and water and electrolyte excretion in the conscious dog. Hypoxic exposure (PIO2 = 56 torr) resulted in a 13% increase in renal blood flow (RBF), while hyperoxic breathing with PIO2 of 700, 1426, or 2139 torr, all resulted in significant 5--7% decline in RBF, a response that was significantly attenuated compared to the striking renal vasoconstriction caused by hyperoxia in anesthetized dogs. Hyperbaric oxygenation (HBO) (1426 torr O2, 2139 torr O2) was associated with unexpected decreases in urine flow (V) of 61% and 70%, respectively. The antidiuresis and mild hemodynamic adjustments were correlated with a 67% decline in urinary PGE2 excretion (UPGE2 x V) when the dogs breathed 700 torr O2, while exposure to 1426 torr O2 and 2139 torr O2 diminished UPGE2 x V by 92% and 99%, respectively. Plasma antidiuretic hormone (ADH) concentration, measured during exposure to 1426 torr O2, was unchanged. In addition, this nonpharmacologic hyperbaric decline in PGE2 excretion was not associated with any changes in sodium excretion of renin secretion, in contrast to the usual depression of these variables with pharmacologic PG inhibition (indomethacin). The HBO antidiuresis may be a consequence of an increased medullary osmotic gradient secondary to reduced vasa recta blood flow. Alternatively, this antiduresis could occur as a consequence of a lowering of the normal functional antagonism existing between PGE2 and ADH, such that the influence of endogenous ADH is potentiated.

Animals↗
PubMed1979

Functional characteristics of monocytes. II. Further observations on lymphocyte-monocyte collaboration in the response to phytomitogens.

Monocytes play a crucial role in the response of lymphocytes to phytomitogens. This role is evident during the very early events after exposure to the mitogen. Thus, significant lymphocyte transformation does occur when monocytes are removed from the culture within a few hours after exposure to mitogen, and the presence of monocytes after the initial period is no longer necessary. Monocytes appear to be required for the early increase in protein synthesis and burst in RNA synthesis following exposure to the mitogen. Monocytes may help in lymphocyte responses partly by longer range, by way of release of soluble humoral factors into culture supernatant fluids. Temperature dependence of the effect of pulse exposure of lymphocytes to these supernatants raises the possibility that membrane receptors on these cells to humoral factors released by monocytes may exist. Moncytes do not appear to act primarily by preserving the viability of lymphocytes in culture.

Cells, Cultured↗